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Bone marrow mesenchymal stem cell-derived exosomes attenuate cardiac hypertrophy and fibrosis in pressure overload induced remodeling.
In Vitro Cellular & Developmental Biology - Animal ( IF 2.1 ) Pub Date : 2020-08-03 , DOI: 10.1007/s11626-020-00481-2
Fu Chen 1 , Xueling Li 1 , Jinxuan Zhao 1 , Jin Geng 2 , Jun Xie 1 , Biao Xu 1
Affiliation  

The multiple therapeutic effects of bone marrow mesenchymal stem cells (BM-MSCs) have been verified in ischemic and reperfusion diseases. Exosomes are thought to play vital roles in MSCs-related cardioprotective effects. Recently, more and more evidences indicated that apoptosis and fibrosis were crucial pathological mechanisms in cardiac remodeling. Whether MSCs-derived exosomes could regulate cardiac hypertrophy and remodeling need to be explored. Murine BM-MSCs-derived exosomes were isolated by differential gradient centrifugation method. The transverse aortic constriction (TAC) mice model was established to promote cardiac remodeling. Cardiac function and remodeling were assessed via echocardiography and histology analysis. Myocytes apoptosis was determined by TUNEL fluorescence staining. Meanwhile, premature senescence was detected by β-galactosidase (SA-β-gal) staining. Related proteins and mRNA alternation were assessed via western blotting and quantitative reverse transcription polymerase chain reaction, respectively. MSCs-derived exosomes significantly protected myocardium against cardiac hypertrophy, attenuated myocardial apoptosis, and fibrosis and preserved heart function when pressure overload. In cultured myocytes, MSCs-derived exosomes also prevented cell hypertrophy stimulated with angiotensin II. One the other hand, exosomes promoted premature senescence of myofibroblasts vitro, indicating its anti-fibrosis effect in cardiac remodeling. Exosomes protected cardiomyocytes against pathological hypertrophy. It may provide a promising future treatment for heart failure.



中文翻译:

骨髓间充质干细胞来源的外来体在压力超负荷引起的重塑中减轻心脏肥大和纤维化。

骨髓间充质干细胞(BM-MSC)的多种治疗作用已在缺血和再灌注疾病中得到证实。外泌体被认为在与MSCs相关的心脏保护作用中起着至关重要的作用。最近,越来越多的证据表明细胞凋亡和纤维化是心脏重塑的关键病理机制。MSCs的外泌体是否可以调节心脏肥大和重塑尚待探索。通过差速梯度离心法分离鼠BM-MSCs来源的外来体。建立横向主动脉缩窄(TAC)小鼠模型以促进心脏重塑。通过超声心动图和组织学分析评估心脏功能和重塑。通过TUNEL荧光染色确定心肌细胞的凋亡。与此同时,通过β-半乳糖苷酶(SA-β-gal)染色检测到早衰。通过蛋白质印迹和定量逆转录聚合酶链反应分别评估相关蛋白和mRNA的交替。当压力超负荷时,MSCs衍生的外来体可显着保护心肌免受心肌肥大,减弱心肌细胞凋亡和纤维化,并保留心脏功能。在培养的心肌细胞中,MSCs衍生的外来体也可以预防血管紧张素II刺激的细胞肥大。另一方面,外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。通过蛋白质印迹和定量逆转录聚合酶链反应分别评估相关蛋白和mRNA的交替。当压力超负荷时,MSCs衍生的外来体可显着保护心肌免受心肌肥大,减弱心肌细胞凋亡和纤维化,并保留心脏功能。在培养的心肌细胞中,MSCs衍生的外来体也可以预防血管紧张素II刺激的细胞肥大。另一方面,外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。通过蛋白质印迹和定量逆转录聚合酶链反应分别评估相关蛋白和mRNA的交替。当压力超负荷时,MSCs衍生的外来体可显着保护心肌免受心肌肥大,减弱心肌细胞凋亡和纤维化,并保留心脏功能。在培养的心肌细胞中,MSCs衍生的外来体也可以预防血管紧张素II刺激的细胞肥大。另一方面,外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。当压力超负荷时,MSCs衍生的外来体可显着保护心肌免受心肌肥大,减弱心肌细胞凋亡和纤维化,并保留心脏功能。在培养的心肌细胞中,MSCs衍生的外来体也可以预防血管紧张素II刺激的细胞肥大。另一方面,外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。当压力超负荷时,MSCs衍生的外来体可显着保护心肌免受心肌肥大,减弱心肌细胞凋亡和纤维化,并保留心脏功能。在培养的心肌细胞中,MSCs衍生的外来体也可以预防血管紧张素II刺激的细胞肥大。另一方面,外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。外泌体在体外促进成纤维细胞的过早衰老,表明其在心脏重塑中具有抗纤维化作用。外泌体保护心肌细胞免于病理性肥大。它可能为心力衰竭提供有希望的未来治疗方法。

更新日期:2020-08-04
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